Oxidative Stress Induced by Iodoacetamide (An Emerging Disinfection By-Product) on HepG-2 Cells

Junbiao Hua,1, Minjie Chenb1, Huan Wub, Lili Zhengb, Qinglan Zhangb, Xiaoling Zhoub*

a Jinhua People’s Hospital, Jinhua, China

b College of Geography and Environmental Science, Zhejiang Normal University,   Jinhua, China

1 Equal contribution and co-first author

*Corresponding author: Tel: +86 (0579) 82282273; 

E-mail address: zhouxiaoling@zjnu.cn

Keywords: Iodoacetamide; HepG-2 cell; oxidative stress; oxidative damage; gene expression 

Submitted: June 12, 2022
Reviewed: October 9, 2022
Accepted: November 13, 2022
Published: January 28, 2023

DOI: 10.14294/WATER.2022.4



Iodoacetamide (IAcAm) is a type of emerging nitrogenous disinfection by-product (N-DBP) with high health risk. Up to now, several studies have been carried out on the toxicity of IAcAm, but the study on oxidative damage of IAcAm on human cells was not available. In this study, the oxidative stress and damage induced by IAcAm on HepG-2 cells were investigated. Results showed that superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity exhibited a decreasing trend; but nuclear factor erythroid 2-related factor 2 (NRF2) and glutamate cysteine ligase catalytic subunit (GCLC), both the mRNA and protein level, generally appeared an increasing trend with the increase of IAcAm concentration. These results suggested that IAcAm-exposed cells produced excessive reactive oxygen species (ROS) and initiated the compensation mechanism of NRF2 to deal with oxidative stress. Malonaldehyde (MDA), an index for oxidative damage, had no obvious change at 24 h (p>0.05) but significantly increased at 48 h (p<0.05). This result indicated that HepG-2 cells could protect themselves from ROS attack by consuming antioxidant enzyme (e.g., SOD and GSH-Px) and upregulating the genes related to antioxidation after 24 h exposure of IAcAm; yet, at 48 h, the antioxidant defense system could no longer prevent oxidative damage of ROS, causing severe damage of the lipid membrane.  

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